[Experimental treatment of smoke inhalation injury with anti-lipid peroxidation agents]

The role of oxygen free radicals in the mechanism of lung damage after smoke inhalation injury was investigated. 42 dogs were used and equally divided into control and treated group. In treated group, a comprehensive anti-lipid peroxidation treatment including Ginseng-ophiopgon, hydrocortisone sodium succinate, Vit. C and E were used at 5 min, 6 hr, and 12 hr postinjury. SOD activity in blood, hypoxanthine, xanthine, uric acid, MDA and SCL in plasma, C2H6 and C2H4 in exhaled breath of dogs after smoke inhalation injury were measured. In addition, blood gas analysis and EVLW were determined to evaluate the lung damage. The results demonstrated that the injured dogs suffered from lung edema and acute lung dysfunction. MDA, SCL in plasma and C2H6, C2H4 in exhaled breath increased markedly, reaching their first peaks at 30 min. and second peaks at 24-72 hours postinjury. The values revealing in first peak in treated group were lower than that in control group. The increase of SOD activity, however, was higher in treated group than in control group. Changes of oxygen free radicals and lipid peroxidation were closely related to lung damage and respiratory dysfunction. These data showed that in early postinjury period increase of oxygen free radicals and excessive lipid peroxidation existed in lungs of dogs. And in treated group, anti-lipid peroxidation activity was increased and lipid peroxidation was inhibited. Lung damage was improved obviously. It was believed that the first peak of changes in oxygen free radicals and lipid peroxidation was related to the onset of early pulmonary damage and the stress response, and the second peak to the development of pulmonary infection and lung repaired.